Contribuição dos aferentes sinoaórticos nos ajustes renais, cardiovasculares, simpáticos e ventilatórios induzidos por hiperosmolalidade aguda

Abstract

The forebrain is suggested the main sensorial site for monitoring changes in plasma osmolality. In addition to the central mechanisms, it has been suggested that peripheral sensors may participate in the osmoregulation. In the present study we investigated the contribution of the sinoaortic afferents in the physiological mechanisms of regulation of the body fluids tonicity during acute hyperosmolality. In the first part of the study, we explored the participation of sinoaortic afferents in the cardiovascular, renal and autonomic responses induced by hypernatremia. Wistar rats (280-350 g) were anesthetized with halothane (2% in O2) and submitted to sinoaortic denervation (SAD), carotid body removal (CBX) or fictitious surgery, and implantation of cannula in the right femoral artery and vein to blood pressure (BP) recording and substance administration, respectively. In the next day, SAD animals were anesthetized with urethane (1.2 g/kg body weight, i.v.) and instrumentalized for renal sympathetic nerve activity (rSNA) recording. Non-anaesthetized CBX animals were used to BP recording and renal excretion test. The parameters were evaluated in response to intravenous infusion of hypertonic saline (HS) (3 mol/L NaCl, 1.8 mL/kg body weight, in 60 seconds). Renal sympathoinhibition induced by infusion of HS was abolished in SAD rats (SAD: -10.7 ± 5.5% of baseline, vs. control rats: -28.7 ± 4.8% of baseline, 60 minutes after HS, p<0.05). CBX attenuated the pressor response (CBX: 5.7 ± 2.0 mmHg, vs. control: 15.8 ± 2.0 mmHg, 12 minutes after HS; p<0.05) and sodium renal excretion (CBX: 74.9 ± 7.3%, vs. control: 99.7 ± 6.7%, 90 minutes after HS; p<0.05) to HS. These results show that the integrity of the aortic and carotid afferents are essential for autonomic, cardiovascular and renal adjustments induced by acute hypernatremia. In the second part we explored the involvement of the carotid bodies and forebrain in the autonomic and ventilatory responses induced by intra arterial infusion of HS using arterially-perfused in situ rat preparations (male Holtzman rats, 60-100 g). HS infusions (0.17; 0.3; 0.7; 1.5 and 2 mol/L NaCl; 200 µL during 20 seconds each) were performed in accumulative ascending order while thoracic sympathetic, phrenic and carotid sinus nerve activities were recorded. Intra-arterial infusion of 2 mol/L NaCl, produced a modest increase in phrenic burst frequency (5.8 ± 0.9 bpm, vs. Ringer: 0.4 ± 0.2 bpm, p<0.05) and markedly enhanced sympathetic (63.3 ± 8.4%, vs. Ringer: -0.8 ± 1.9%, p<0.05) and carotid sinus nerve activities (105.1 ± 13.2%, vs. Ringer: -0.2 ± 1.3%, p<0.05). Carotid bodies removal attenuated the sympathoexcitation (26.2 ± 4.9%, p<0.05), but not the tachypnea (3.6 ± 0.5 bpm) induced by 2 mol/L NaCl. The forebrain disconnection at the pre-collicular level, abolished the sympathoexcitation (8.4 ± 3.7%, p<0.05) and the increase in phrenic burst frequency (1.2 ± 0.4 bpm, p<0.05) in response to 2 mol/L NaCl. The results indicate the participation of forebrain in the sympathetic and ventilatory responses produced by sodium overload. Moreover, they suggest that carotid bodies may act as a sodium peripheral sensor contributing for the autonomic responses to acute hyperosmotic challenges.